In addition, it was discovered that CSE specifically deficiency in ECs resulted in an increase in the expression of CD62E, which is associated with the activation of ECs and the development of atherosclerosis, and led to an elevated adherence of monocytes even without an inflammatory trigger, along with also accelerated the progression of endothelial dysfunction and atherosclerosis; but these effects were restored when treated with H2S donor. Here, SELE is linked to atherosclerosis.